The present invention relates to “implantable medical devices” such as those defined by the Jun. 20, 1990 Directive 90/385/EEC of the Council of European Communities, specifically to implantable devices that continuously monitor heart rhythm and deliver to the heart, if necessary, electrical stimulation pulses for cardiac resynchronization and/or defibrillation, in response to an arrhythmia detected by the device. The present invention relates more particularly to those devices that deliver an anti-tachycardia pacing (“ATP”) therapy, that is a programmed high-frequency stimulation of the atrium, or a pulse train of stimulations (notably including 30 Hz stimulation. WO95/03086 A1 discloses such an implanted device able to deliver if necessary an ATP stimulation to the patient.
ATP therapy is indicated to treat certain arrhythmias caused by disturbances of the action potentials in the atrium. Therapy by stimulation of the atrium can be applied in case of detection of an abnormal fast heart rhythm of atrial origin (atrial fibrillation or other atrial arrhythmia). It will be called hereinafter “antitachycardia atrial pacing” (also referred to as “ATP-A”).
Overall, the decision to apply antitachycardia therapy, and the choice of this therapy (whether an application of a defibrillation shock, or an ATP therapy or a similar type antitachycardia stimulation) is made by an algorithm for detecting and classifying different tachyarrhythmias based on several discrimination criteria. These criteria include, for example, the ventricular rate, the stability of ventricular intervals (namely, RR intervals), the analysis of the atrioventricular association revealed by the stability of the PR interval, and the start-up mode of the tachycardia (presence of an abrupt acceleration and identity of the cavity of origin, ventricular or atrial).
Some of these tachycardias can be treated by activating an antitachycardia atrial pacing (ATP-A).
However, when an antitachycardia pacing in the atrium therapy is delivered, the device is unable to detect ventricular events. This is because the duration of the post atrial pacing ventricular refractory periods, relative to the interval between two consecutive atrial stimulations, effectively blocks any detection of any ventricular depolarization.
Further, ventricular contractions during these arrhythmia episodes can be very irregular or even non-existent, causing the onset of ventricular pauses. It is therefore important to maintain a detection of the ventricular activity during the application of antitachycardia atrial pacing so as, if necessary, to stimulate the ventricle if no spontaneous ventricular event is detected. As will be discussed below, the term “antibradycardia ventricular pacing” refers to this conditional stimulation of the ventricle.
More specifically, disturbances of the atrium and/or ventricle action potentials can cause ventricular arrhythmias. These are generally classified as Supraventricular Tachycardias (SVT) or Ventricular Tachycardias (VT). The SVT is characterized by an abnormal rhythm in the atrium or at the atrioventricular node. The most common SVTs are atrial flutters and atrial fibrillations:
During atrial flutters, the action potentials have a circular atrial path, causing an acceleration of the rate of contraction of the atrium with atrioventricular intermittent conduction (2:1 or 3:1, for example);
As for atrial fibrillation, these are common arrhythmias that correspond to uncontrolled atrial depolarization, leading to a sometimes rapid and often irregular activity of the ventricles thereby reducing the hemodynamics efficiency of the ventricular contraction.
During these atrial arrhythmias, the patient may experience palpitations and complain of malaises, dyspnoea and chest pains. It can be important to treat these arrhythmias in some cases, and the application of antitachycardia pacing is one treatment option.
However, in the presence of a stimulation of the atrium—and thus, especially during the application of an antitachycardia atrial pacing therapy—the electrical detection of the ventricular activity by the device can be masked by the atrial post-stimulation refractory periods.
One solution to this masking problem is to always deliver a ventricular pacing for the duration of the antitachycardia atrial pacing therapy. However, such a ventricular stimulation will always be an asynchronous pacing, because of the refractory periods subsequent to the stimulation and the blanking periods, corresponding to the disconnection of the detection circuits of the amplifier to allow the discharge of the stored energy in the heart at the heart/electrode inter face after stimulation. Because of this asynchrony, there is a risk of stimulating a T wave, with the possible consequence of triggering ventricular arrhythmias.